Human eosinophils release matrix metalloproteinase-9 on stimulation with TNF-α☆☆☆★

Schwingshackl, Andreas; Duszyk, Marek; Brown, Norman D.; Moqbel, Redwan

doi:10.1016/s0091-6749(99)70079-5

Cited by 119 publications

(68 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, MMP-9 and eotaxin-2 were decreased in the peritoneal cavity of Thy-1 À/À mice upon induction of inflammation by thioglycollate. As shown by other groups, we also detected these products in granulocytes or monocytes by RT-PCR [33][34][35][36][37]. Thus, the decreased number of granulocytes and macrophages in Thy-1 À/À mice might be directly responsible for the reduced levels of these cytokines, chemokines, and protease in the BAL or peritoneal fluid of Thy-1 À/À mice.…”

Section: Discussionsupporting

confidence: 78%

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

View full text Add to dashboard Cite

Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung inflammation, the influx of eosinophils and monocytes was also strongly decreased. These effects were independent of Thy-1 expression on T cells, as shown by the transplantation of WT BM into the Thy-1-deficient mice. In spite of the strong Thy-1 expression on T cells in the chimeric mice, the extravasation of the inflammatory cells in these mice was significantly diminished, compared to control mice. Finally, the altered number and composition of infiltrating leukocytes in Thy-1-deficient mice modified the chemokine/cytokine and protease expression at the site of inflammation. In conclusion, Thy-1 is involved in the control of inflammatory cell recruitment and, thus, also in conditioning the inflammatory microenvironment.Key words: Extravasation . Inflammation . Thy-1 Supporting Information available online IntroductionThe recruitment of inflammatory cells to sites of inflammation plays an important role in the pathogenesis of several inflammatory diseases. Leukocyte adhesion to endothelial cells (ECs) follows a multistep process, including the capture of free leukocytes out of the blood stream, rolling, firm adhesion, and transendothelial diapedesis. The importance of several adhesion molecules in this series of events has been described previously [1]. In ICAM-1-deficient mice, neutrophil recruitment was significantly reduced, but it was not completely blocked in a chemical peritonitis model or in a lipopolysaccharide 645(LPS)-induced airway inflammation model, indicating the involvement of additional adhesion molecules [2,3]. Furthermore, leukocyte recruitment in experimental colitis was not affected by blocking ICAM-1 or MadCAM, whereas the blocking of VCAM-1 resulted in a significant attenuation of colitis [4]. Thus, under specific inflammatory conditions, certain adhesion molecules mediate adhesion and transmigration of leukocytes into the perivascular tissue.Recently, human Thy-1 expressed on ECs was identified as an adhesion molecule mediating the binding of neutrophils and monocytes to activated microvascular ECs [5]. Thy-1 is a highly glycosylated GPI-anchored surface protein and a member of the immunoglobulin superfamily [6,7,8]. In humans, Thy-1 is expressed on ECs at sites of inflammation or in tumours whereas ECs do not express Thy-1 in healthy tissue [5,9]. Thy-1 is also expressed on fibroblasts, neurons, and a su...

show abstract

Section: Discussionsupporting

confidence: 78%

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

View full text Add to dashboard Cite

show abstract

“…In addition, eosinophils are known to be a major source of MMP-9 [31]. Given that MMP-9 levels are increased during eosinophil-mediated inflammatory processes, such as bronchial asthma [32,33] and TDI-OA [34], it is not surprising that MMP-9 levels were correlated with sputum eosinophil count in the present study. VEGF is the most potent direct-acting regulator of angiogenesis, and its level of expression is often excessive in chronic inflammation [35].…”

Section: Discussionsupporting

confidence: 50%

Histamine Release and Inflammatory Cell Infiltration in Airway Mucosa in Methylene Diphenyl Diisocyanate (MDI)-Induced Occupational Asthma

et al. 2008

View full text Add to dashboard Cite

Introduction Although methylene diphenyl diisocyanate (MDI) is widely used in industries, there have been few studies of the pathogenic mechanisms of MDI-induced occupational asthma (MDI-OA). Methods We performed immunohistochemical analyses, measured inflammatory mediators and cytokines, and quantified histamine release (HR) from peripheral basophils in MDI-OA patients. Thirteen MDI-exposed workers (five MDI-OA, two MDI-induced esoinophilic bronchitis, and six asymptomatic exposed controls, AEC) were enrolled. Results and Discussion Immunochemical analyses indicated significantly increased anti-eosinophilic cationic proteinstained cells in MDI-OA patients as compared with controls (P<0.05). Sputum eosinophil cationic protein levels were increased after MDI-specific inhalation challenge test in MDI-OA/EB patients (P<0.02). Sputum eosinophil counts were highly correlated with IL-8 and MMP-9 levels (P<0.05 and P<0.01, respectively). Basophil HR was significantly increased in MDI-OA patients after stimulations with anti-IgG4 and MDI-human serum albumin conjugates (both P<0.05). Eosinophil activation is a major feature of airway inflammation in MDI-OA patients. Increased HR by MDI may contribute to the pathogenic mechanisms of MDI-OA.

show abstract

“…The number of TNF-␣-positive cells (41) and the concentration of TNF-␣ 18 h after segmental Ag challenge in bronchoalveolar lavage fluid are increased in asthmatic airways (42). Moreover, TNF-␣ is known to increase MMP-9 release by monocyte/macrophages (43,44) and eosinophils (45). Therefore, we hypothesized that TNF-␣ stimulates MMP-9 and tenascin release from bronchial fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Ets-1 Regulates TNF-α-Induced Matrix Metalloproteinase-9 and Tenascin Expression in Primary Bronchial Fibroblasts

Nakamura

Esnault

Maeda

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

Increased subepithelial deposition of extracellular matrix proteins is a key feature in bronchial asthma. Matrix metalloproteinase-9 (MMP-9) is a proteolytic enzyme that degrades the extracellular matrix. Tenascin is an extracellular matrix glycoprotein that is abundant in thickened asthmatic subbasement membrane. The expression of MMP-9 and tenascin reflects disease activity in asthma and airway remodeling. The molecular mechanisms regulating the expression of these proteins remain unknown. Both MMP-9 and tenascin promoters contain an Ets binding site, suggesting control by Ets-1. Thus, we hypothesized that Ets-1 expression is increased in asthma and that it contributed to enhanced MMP-9 and tenascin expression. To test this hypothesis, we determined the expression of Ets-1 in bronchial biopsies obtained from asthmatic subjects and determined the expression of Ets-1, MMP-9, and tenascin by bronchial fibroblasts activated ex vivo. We observed that nuclear extracts from TNF-α-activated fibroblasts showed increased Ets-binding activity. In addition, TNF-α-activated fibroblasts had increased expression of Ets-1 mRNA and protein, which preceded an increase in MMP-9 and tenascin mRNA. Furthermore, treatment of fibroblasts with Ets-1 antisense oligonucleotides down-regulated TNF-α-induced Ets-1, MMP-9, and, to a lesser extent, tenascin protein expression or activity. Taken together, these data demonstrate that TNF-α increases MMP-9 and tenascin expression in bronchial fibroblasts via the transcription factor Ets-1, and suggest a role for Ets-1 in airway remodeling in asthma.

show abstract

Human eosinophils release matrix metalloproteinase-9 on stimulation with TNF-α☆☆☆★

Cited by 119 publications

References 41 publications

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Histamine Release and Inflammatory Cell Infiltration in Airway Mucosa in Methylene Diphenyl Diisocyanate (MDI)-Induced Occupational Asthma

Ets-1 Regulates TNF-α-Induced Matrix Metalloproteinase-9 and Tenascin Expression in Primary Bronchial Fibroblasts

Contact Info

Product

Resources

About